Pharmacodynamics: How Caffeine Helps Burn Fat
The mechanism of action, that is, the pharmacodynamics of sodium caffeine-benzoate, is based on several biochemical processes. First, caffeine depresses the effector cell enzyme phosphodiesterase, which regulates the transfer of intracellular signals, and this is reflected in an increase in the concentration of the cAMP-cyclic adenosine monophosphate generating hormone. As a result, cAMP increases the activity of fat cell enzymes (adipocytes) that break down triglycerides, and thus the intensity of lipolysis in cells of visceral adipose tissue increases.
An important role is played by the similarity of the chemical structure of caffeine (the methylated purine base of xanthine) to the molecular structure of the adenosine produced by the body, a purine neurotransmitter that inhibits brain excitation. Molecules of caffeine can bind to adenosine receptors in brain cells and do not allow them to activate, that is, they act as a competitive antagonist. But for the fat burning process, the key is that this antagonism promotes the release and activation of catecholamine neurotransmitters, including adrenaline.
Adrenaline acts on membrane adrenoreceptors of adipose tissue cells and also stimulates enzymes involved in the cleavage of triglycerides.
In addition, the effect of caffeine in diet pills is associated with its diuretic effect, which arises from the inhibition of water reabsorption in the renal tubules. However, an increase in the volume of urine is observed only with a dose of caffeine of more than 300 mg.
Caffeine, like most psychostimulants, suppresses appetite, that is, delays the signal of hunger, but the mechanism of this effect is not yet known.